Loss of G protein pathway suppressor 2 in human adipocytes triggers lipid remodeling through upregulation of ATP binding cassette subfamily G member 1
Ontology highlight
ABSTRACT: Here we demonstrate that the loss of GPS2 triggers the reprogramming of cellular processes related to adipocyte differentiation by increasing the responses to the adipogenic cocktail. Moreover, GPS2-depleted human adipocytes are characterized by hypertrophy, triglyceride and phospholipid accumulation, and sphingomyelin depletion. These changes are likely a consequence of the increased expression of ATP-Binding cassette subfamily G member 1 (ABCG1) that mediates sphingomyelin efflux from adipocytes and modulates lipoprotein lipase (LPL) activity. We identify ABCG1 as a direct transcriptional target, as GPS2 depletion leads to coordinated changes of transcription and H3K27 acetylation at promoter and enhancers which are occupied by GPS2 in wild-type adipocytes. Finally, we find that in omental adipose tissue of obese humans GPS2 levels correlate with ABCG1 levels, type 2 diabetic status, and lipid metabolic status.
ORGANISM(S): Homo sapiens
PROVIDER: GSE152517 | GEO | 2020/08/28
REPOSITORIES: GEO
ACCESS DATA